Gaetano Gentile

Effects of Heart Rate Changes on Arterial Distensibility in Humans

Abstract—In rats, an increase in heart rate by pacing is accompanied by progressive large-artery stiffening. Whether this is also the case in humans is unknown. We enrolled 20 patients who were chronically implanted with a pacemaker because of atrioventricular block or sick sinus syndrome. Arterial distensibility was measured by an echo-tracking device. In 10 patients, the evaluation was performed on the radial artery by using continuous finger blood pressure measurements, whereas in the remaining 10 patients, the common carotid artery was studied with a semiautomatic measure of brachial artery blood pressure. Diastolic diameter, systodiastolic diameter change, and distensibility were obtained at baseline (heart rate 63±2 beats/min) and after atrial and ventricular sequential pacing at a heart rate of 90 and 110 beats/min. At baseline, the diameter was 7.8±0.3 mm in the carotid artery and 2.4±0.1 mm in the radial artery; the respective systodiastolic diameter change values were 375.4±31.0 and 55.9±9.0 (&mgr;m) and the distensibility values were 1.4±0.1 and 0.7±0.1 (1/mm Hg 10−3). Blood pressure and diameter were not significantly modified by increasing heart rate, which markedly modified systodiastolic diameter change and distensibility. In the radial artery, distensibility was reduced by 47% (P <0.05) at a heart rate of 90 beats/min with no further reduction at 110 beats/min. In the carotid artery, distensibility was reduced by 20% at a heart rate of 90 beats/min (P <0.05) with a further reduction at 110 beats/min (45%, P <0.05). These data provide the first evidence in humans that acute increases in heart rate markedly affect arterial distensibility and that this occurs in both large- and middle-size muscle arteries within the range of “normal” heart rate values.

Acute Effect of High-Fat Meal on Endothelial Function in Moderately Dyslipidemic Subjects

Objective— Hypercholesterolemia markedly impairs endothelial function. Whether this is the case for hypertriglyceridemia is less clear, however, and limited evidence exists on the effect of an acute increase in triglyceridemia caused by a high-fat meal. Methods and Results— In 16 normotensive subjects with an untreated mild hypertriglyceridemia and dyslipidemia and in 7 normal controls, we measured radial artery diameter and blood flow by an echo-tracking device (NIUS02). Data were obtained at baseline, at the release of a 4-minute ischemia of the hand, which causes an increase in arterial diameter dependent on nitric oxide (NO) secretion, and at the release of a 12-minute exclusion of the arm by an arm cuff to obtain a larger increase in arterial diameter mainly of nonendothelial nature. Measurements were performed before and 6 hours after a high-fat meal (680 kcal/m2 body surface; 82% lipids). In mild dyslipidemic hypertriglyceridemic subjects, the high-fat meal did not alter baseline blood pressure (beat-to-beat finger measurement), heart rate, radial artery diameter, and blood flow. It also did not alter the increase in blood flow induced by the 4-minute ischemia (+42.7±10.4 and +43.7±10.4 mL/min), whereas it markedly attenuated the concomitant increase in arterial diameter (+0.31±0.06 versus 0.13±0.06 mm; P<0.05). The alteration of the diameter response did not correlate with changes in total cholesterol, but it showed a significant correlation with the increase in serum triglycerides induced by high-fat meal (r=0.49, P<0.05). This attenuation was not seen in control subjects and in subjects in whom measurements were repeated after a 6-hour observation period. It was also not paralleled by an alteration of the endothelially independent response to a 12-minute ischemia whose larger effects on arterial diameter and blood flow were similar before and after the high-fat meal. Conclusions— Endothelial function is markedly impaired by a high-fat meal that causes an acute hypertriglyceridemia. This impairment is evident in dyslipidemic patients with baseline hypertriglyceridemia but not in normotriglyceridemic controls.

Effects of heart rate changes on arterial distensibility in humans - Response

Effects of Heart Rate Changes on Arterial Distensibility in Humans To the Editor: Dependence of arterial stiffness on heart rate, claimed by Giannattasio et al,1 runs counter to classic studies, which were previously discussed in relation to conflicting data obtained with one method used to measure aortic pulse wave velocity.2 There is a potential flaw in the method applied by Giannattasio et al in their determination of carotid and radial artery distensibility at different heart rates. They measured diameter change of the target artery, but pressure pulsation at a distal site (brachial pressure for carotid, finger pressure for radial artery). Errors inherent in distal pressure measurement have been stressed in a recent consensus document3 but were considered by authors1 to be minimal. We disagree. In similar studies by Wilkinson et al,4 there was an average 35% fall in central pulse pressure, compared with brachial, when heart rate was increased from 60 to 110/min by pacing. Giannattasio et al quoted an early evaluation of the Finapres system and considered this accurate for their purposes, but this study did not test response to change in heart rate. In a later manuscript by the developers of Finapres,5 a marked heart rate difference was noted for systolic pressure between noninvasive finger and brachial intraarterial pressure (20 mm Hg difference for heart rate change of 40 bpm). The differences in distensibility calculated by Giannattasio et al were at the margin of statistical significance (P 0.05). Given the problems in estimating pulse pressure at the site of diameter measurement and the likelihood that this was overestimated, we continue to rely on the previous work,2,3 which showed no significant dependence of arterial stiffness on heart rate.

Safety, Efficacy, and Complications of Pericardiocentesis by Real-Time Echo-Monitored Procedure

Pericardiocentesis is useful in the diagnosis and treatment of pericardial effusive disease. To date, a number of methods have been developed to reduce complications and increase the success rate of the procedure. The aim of the present study was to evaluate the efficacy and the safety of echocardiography-guided pericardiocentesis under continuous echocardiographic monitoring in the management of pericardial effusion. We prospectively performed 161 pericardiocentesis procedures in 141 patients admitted from 1993 to 2015 in 3 centers. This procedure was performed for tamponade or large pericardial effusion in 157 cases and for diagnosis in 4 cases. A percutaneous puncture was performed where the largest amount of fluid was detected. To perform a real-time echo-guided procedure, a multi-angle bracket was mounted on the echocardiographic probe to support the needle and enable its continuous visualization during the puncture. The procedure was successful in 160 of 161 cases (99%). Two major complications occurred (1.2%): 1 mediastinal hematoma that required surgical drainage in a patient on anticoagulant therapy and 1 pleuropericardial shunt requiring thoracentesis. Seven minor complications occurred (4.3%): 1 pleuropericardial shunt, 1 case of transient AV type III block, 3 vasovagal reactions (1 with syncope), and 2 cases of acute pulmonary edema managed with medical therapy. No punctures of any cardiac chamber occurred, and emergency surgical drainage was not required in any case. In conclusion, echocardiography-guided pericardiocentesis under continuous visualization is effective, safe, and easy to perform, even in hospitals with low volumes of procedures with or without cardiac surgery.

The role of early contrast-enhanced chest computed tomography in the aetiological diagnosis of patients presenting with cardiac tamponade or large pericardial effusion.

AIMS The role of chest computed tomography (CT) is not well defined for either diagnosis or management of pericardial disease. The aim of this study was to evaluate the added value of early chest CT in the diagnostic workup for patients presenting with cardiac tamponade or large pericardial effusion of unknown aetiology as the first manifestation of disease. METHODS AND RESULTS We performed CT scan on 55 patients with pericardial effusion as defined above, undergoing echo-guided pericardiocentesis. We compared the success rate in making diagnosis and/or staging the underlying disorder of three sequential workups, including, respectively, (i) clinical presentation, inflammatory markers, chest X-ray imaging, (ii) all of the above and pericardial fluid analysis, and (iii) all of the above and chest CT. We were able to make diagnosis in 53 patients (96%): the major cause of effusion was malignancy (38%). Clinical and biochemical data were not able to differentiate non-tumour from tumour patients. CT revealed pathological findings in all patients with malignancy: tumour mass in 15/21 (71%) and pathological lymphadenopathy in the remaining 6 cases. The workup including CT provided a significantly higher diagnostic yield than the other two workups (P < 0.0001), both in the overall population and in the two subgroups of neoplastic (Npl) and non-Npl patients. CONCLUSION In all patients with cardiac tamponade or large pericardial effusion, CT was useful either in identifying the underlying disease or in excluding other potential causes of pericardial effusion. We conclude that chest CT is a very useful non-invasive diagnostic tool to identify and stage pericardial diseases.

Sinoatrial Blocks in Hyperthyroidism Treated with Beta-Blockers: A Case of Paradoxical Treatment

We describe an interesting case of a 52 year-old patient affected by thyrotoxicosis crisis, in whom sinoatrial blocks were associated with syncope and treated effi ciently with beta-blockers.

Aborted sudden death from Epstein-Barr myocarditis.

To the Editor Ventricular fibrillation is the most common ECG pattern of presentation in adult cardiac arrest and usually has an ischemic origin. Cardiomyopathy and channelopathy are more frequent in the youngest adult group. Among the transient causes of ventricular fibrillation one should also keep viral myocarditis in mind. Epstein–Barr has rarely been reported as a cause of acute myocarditis, accounting for about 1% of cases, but has been associated with complete heart block, ventricular arrhythmias, myocardial infarction-like patterns and sudden death. The infection may occur with the typical mononucleosis syndrome characterized by the triad of fever, pharyngitis and lymphadenopathy, but cardiac manifestation may be the first sign of virus diffusion and can include any of the following: chest pain, dispnea, palpitation or sudden cardiac death.

P-35: Response and compliance of hypertensives to treatment by device-guided breathing exercises: Interim results

Previous studies have demonstrated a sustained reduction of high blood pressure (BP) with device guided breathing exercises. We are evaluating compliance & performance of patients using “treat & measure” devices at home and the possible occurrence of placebo effect. Me hods: Patients, were uncontrolled hypertensives, age 30 to 65 either unmedicated or medicated with antihypertensive drugs. The design includes 4 visits (#1 to #4) at the office defining a 2-weeks baseline (#1 to #2) followed by an 8-weeks treatment phase (#2 to #4) with follow up at #3. Self treatment takes place at home 15 minutes every evening using the RESPeRATE device (InterCure Ltd., Israel), which guides the user interactively to slow breathing while storing automatically compliance & performance data. BP & heart rate (HR) are measured at both office & home using a digital BP monitor with automatic data logging (A&D, Japan). Self measurements at home are applied every morning between visits #1 to #4. Outcomes are average BP & HR changes from Baseline (applied over visits #1[0002] for “office” and daily for “home”) to “End” (visit #4 for “office” and last 3 treatment weeks for “home”). Compliance & performance are evaluated using data logged by the devices. Placebo effect during baseline is tested by linear regression of daily averaged BP & HR changes during Baseline. The time course of home BP changes from baseline by nonlinear regression using a logistic function. Results: Interim analysis of the first 17 treated patients with available outcomes shows that patient were compliant in both BP measurements and treatment and were able to achieve slow breathing, as required. Significant systolic & diastolic BP reduction was observed in response to treatment for both “office” (from 141616/8866 to 125611/8169 mmHg with p,0.01) and “home” (from 133 68/8269 to 12568/7768 mmHg with p,0.0001) with no significant HR changes (69 to 67 at “office” and 68 to 70 at “home”). No placebo effect was observed during baseline. The home BP reduction was developed in 2 to 5 treatment weeks and then reached a plateau. Conclusion: Self-treatment of hypertension by device-guided breathing exercises with self-BP monitoring at home is technically feasible and enables objective quantification of the patients compliance and performance as well as time course of the BP response.